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There is an imbalance between lipid peroxidation and serum vitamin E levels in pre-eclampsia and eclampsia. Increased lipid peroxidation is well correlated with the increase in systolic and diastolic BP measurements and serum uric acid levels.

The effects of ethanol consumption on the levels of lipid peroxidation (TBARS) and reduced glutathione (GSH) in the brain stem of male rats were investigated. The rats randomly divided into eight groups: control, 10%, 25%, 35% ethanol-consuming groups and four groups given vitamin E. Brain stem GSH levels were significantly decreased by 39.74%, 61.57%, 78.23% in rats consuming 10%, 25% and 35% ethanol, respectively. The level of TBARS was increased six-fold, 12-fold and 17-fold in these groups when compared with the control group. The administration of vitamin E (100 mg/kg/day, i.p) to ethanol-consuming rats for 20 days caused a significant increase in glutathione levels and a significant decrease in lipid peroxidation.

Background: Genome-wide association studies (GWAS) implicate single nucleotide polymorphisms (SNPs) on chromosome 6p21.3-22.1, the human leukocyte antigen (HLA) region, as common risk factors for schizophrenia (SZ). Other studies implicate viral and protozoan exposure. Our study tests chromosome 6p SNPs for effects on SZ risk with and without exposure. Method: GWASsignificant SNPs and ancestry-informative marker SNPs were analyzed among African American patients with SZ (n = 604) and controls (n = 404). Exposure to herpes simplex virus, type 1 (HSV-1), cytomegalovirus (CMV), and Toxoplasma gondii (TOX) was assayed using specific antibody assays. Results: Five SNPs were nominally associated with SZ, adjusted for population admixture (P < .05, uncorrected for multiple comparisons). These SNPs were next analyzed in relation to infectious exposure. Multivariate analysis indicated significant association between rs3130297 genotype and HSV-1 exposure; the associated allele was different from the SZ risk allele. Conclusions: We propose a model for the genesis of SZ incorporating genomic variation in the HLA region and neurotropic viral exposure for testing in additional, independent African American samples.

Moderate systemic hypothermia (28 degrees C) appears to protect brain stem tissue from oxidative stress during severe hemorrhagic shock in rats, as indicated by insignificant change in tissue TBARS and GSH concentrations. These results suggest antioxidant protective effects of moderate systemic hypothermia in metabolically active brain stem tissue during hemorrhagic shock. Similar effects in humans remain to be studied.